Podcasts about Parkinsonism

In this episode, Dr. Mahzabin Islam, consultant neurologist, talks us through the clinical examination of Parkinson's disease, approaches to assessing Parkinsonism, as well as recent research updates and the role of diet and lifestyle modifications in Parkinson's disease.

Between 1918 and 1920, the Spanish Flu killed 50 million people worldwide.  This pandemic, arrived on the heels of WW1, and between the two events, nearly 5% of the world's population was killed.  But there was another pandemic occurring, one that is less well known and less frequently talked about, that remains a mystery to this day.  In the winter of 1916 in Europe, people were seeking medical attention for general malaise.  At first, it looked like a mild case of the flu with fever, headaches, and fatigue.  Many would recover, but some would begin exhibiting tremors and many slowed down mentally and physically, until they were completely immobile despite being conscious and alive.  The symptoms presented on a spectrum, but patients sometimes experienced lethargy or even obtundation, paralysis of eye muscles, rigid muscles, frozen posture, loss of speech, and sudden immobility.  In some cases, the progression was overnight.  In others, it took weeks to months.  Doctors called it Encephalitis Lethargica, but no one really understood it.  Some patients slept for days.  Others stayed awake, trapped inside bodies that no longer moved.  Hundreds of thousands of people lost the ability to walk and talk, and then in 1928 new cases just stopped appearing.  By then, however, there had been more than 1 million cases, and half of those had ended in death.  Those that did survive, often developed a post-encephalitic Parkinsonism leaving them rigid, slow, and unable to move normally for the rest of their lives.And then, just as mysteriously as it appeared… it vanished.  So what was this disease? A viral epidemic? A post-war complication? Something we still don't fully understand?  This week, we're diving into one of the most unsettling medical mysteries in modern history, Encephalitis Lethargica, also known as the Sleeping Sickness.Send us Fan MailSupport the showTheme song by INDA

Tune in to The Other Side Of Midnight, the wildest late-night talk show on the airwaves, where absolutely no topic is off-limits. Host Walter Sterling dives deep into the cultural impact of actress Sydney Sweeney, arguing she single-handedly restored "sexual order" and inspired a generation of young men to return to church. He also rants about the absurdity of COVID-19 mandates and shares a shocking personal story of his own vaccine-triggered Parkinsonism misdiagnosis. Plus, buckle up for "Florida Stories," a hilarious roundup of the Sunshine State's most bizarre "hold my beer" moments, featuring everything from porta-potty crashes and trading weed at the McDonald's drive-thru to dodging bears with donuts. From Hollywood gossip and live calls with midnight misfits to declaring the undeniable supremacy of New Jersey pizza, this is your perfect, chaotic companion for the other side of midnight Learn more about your ad choices. Visit megaphone.fm/adchoices

In this episode, we explore how individualised medicines are evolving from “n=1” treatments (a treatment effective for a single individual) into approaches that could transform care for many people living with rare conditions.  Advances in genomic medicine are making it possible to design highly targeted treatments based on an individual's genetic information. While these therapies may begin as bespoke solutions for a single patient, they can often be adapted, refined or reused to benefit others with similar conditions.  While the research is evolving, the systems needed to deliver these treatments at scale are still catching up. From regulation to access, our guests discuss what needs to change to turn this potential into reality.  Our host Sharon Jones, is joined by:  Ana Lisa Tavares, Clinical Lead for Rare Disease Research at Genomics England  Mel Dixon, Participant Panel member and CEO and Founder of Cure DHDDS  If you enjoyed today's conversation, please like and share wherever you listen to your podcasts.  “However rare your condition is, someone has a right to have hope. Everybody should have a hope that we should be able to find a treatment.” You can download the transcript or read it below. Sharon: What if treatments once designed for just one person could now help many others? Thanks to advances in genomic medicine, regulations are changing and research is expanding. This opens up more options for treatments for rare conditions. But what does this mean and how close is real change? I'm Sharon Jones, and this is Behind the Genes. We look at how genomics is changing healthcare, covering everything from cutting-edge research to real-life stories. Individualised medicines are a fast-moving area, but there's still a big gap between scientific progress and what's actually happening to patients. You could call it the gap between hype and hope. Ana Lisa: However rare your condition is, someone has a right to have hope. Everybody should have a hope that we should be able to find a treatment. Sharon: Coming up, we'll hear from Ana Lisa Tavares, Clinical Lead for Rare Disease Research at Genomics England, and Consultant in Clinical Genetics at Cambridge University Hospital, as well as Mel Dixon, member of the Participant Panel at Genomics England and CEO and founder of Cure DHDDS. Mel opens this chat by explaining why developments in individualised healthcare really matter to her. Mel: This issue is really personal to me. I have three children, two of whom are affected with an ultra-rare DHDDS gene variant, for which there is currently no treatment. Their condition causes symptoms such as, well, it varies between mild to severe learning difficulties, seizures, tremors, and movement and coordination difficulties. But the, the most worrying thing for us was that this condition is actually also progressive. So over time it becomes more of a Parkinsonism and some patients experience dementia-like symptoms and psychosis. So for us to get a treatment that targets the genetic cause of, of their condition is, like, the most important thing in, in our lives. If we could intervene now, they could potentially, at the stage they're at, you know, live an independent life with, with some supports. But if the disease is left to progress, it would be a very different outcome for them. Sharon: I mean, that sounds so difficult and I can't even imagine how life is for you and your family. And I can see what is driving you to find anything to extend the life of your children and to give them that opportunity to, to have a better quality of life. And then Lisa. Ana Lisa: It's a huge burden for families to carry. And I think at the moment there's an additional layer of burden, which shouldn't fall on families, to feel like they need to forge a pathway for their child to have a chance of a treatment. That's, that's a lot to bear. Mel: I think as well, families feel they almost have to become mini scientists in their children's specific condition overnight, because you go to these appointments with the consultants and nobody's heard of the condition and they don't know, they just don't really know what to do with you. So they're asking you, you know, so tell me about this, this gene change. What, what does it do? What does it mean? So you have to become the mini professor in your child's condition to be able to advocate for them. We've had to really learn on our feet so that we're able to advocate and push for research into DHDDS, because without us doing it, nobody else was going to be. Sharon: Yeah. So that's, you know, that's partly what we're here and what this podcast is for, it's here to support families to, to understand this stuff. And Ana Lisa, can you just break it down to us, what is individualised medicines? Ana Lisa: An individualised medicine that's made for one individual person. In reality, sometimes there are other individuals that can also benefit from the same medicines, and sometimes actually, although the medicine is made for one specific person, it might be made using a strategy that other patients could also benefit from, either directly, exactly the same, even, or through tweaking them so that they could work for a different patient. In the context that they're most often referred to at the moment, they're therapies that are being made based on the genetic information about somebody. Sharon: Thank you. I mean, that sounds amazing. And now coming to you, Mel, what does receiving a diagnosis mean for a family? And how do you navigate the space between finally having answers and the reality that the treatment may not yet exist? Mel: So for us, I think, we went down the, the diagnostic route in the hope that we would be able to find a treatment for our children, or there would already be a treatment in place. But unfortunately when we got their diagnosis, we were told that their, their condition was ultra rare, neurodegenerative and also newly discovered. So there was, there was no treatment pathway and actually minimal research happening into it at the time. So it was frustrating, upsetting, um, and it felt like quite a hopeless situation at the start, but actually this was just over three years ago. And through a lot of proactiveness on our part in fundraising, we've been able to better understand the condition and we now have treatments in the pipeline. So in that three-year window, from there being nothing, we now have treatments both in terms of potential drug repurposing candidates and also, um, an individualised therapy called an ASO is also in development for them. So it was hard, but it's given huge benefit to us. Otherwise, we'd just be going, remaining going from specialist to specialist without having any answers or understanding why their symptoms were progressing. Sharon: I mean, that sounds really, really tough and you know, coming back to you, Ana Lisa, could you talk us through how genomics is changing the way we can treat rare conditions? You know, what types of individualised medicines now exist and how do they even work? Ana Lisa: Maybe I'll start with how some of these medicines are working. So with, without going into details, but the sort of principle that these medicines might be able to, to do something called gene editing. So our, our DNA, uh, the instruction manual is made up of genes and it's now can be possible scientifically to change even a single DNA letter code in somebody to try and ameliorate the symptoms of their rare condition. You know that's phenomenal scientific progress to be able to do that. I think a lot of people have heard about gene therapy, where one is trying to get into the body a gene or part of a gene that might be able to sort of replace the function of a gene that isn't working as it should. There are various other strategies. So our DNA is actually used to send messages to our body, if you like, to, to decode these instructions. And so there are medicines that target the next step in this process, the RNA, which are the ASO therapies that Mel was referring to earlier. And really what those are doing are either trying to correct for a protein in our body that isn't working as it should, or to try and get rid of one that shouldn't be there. And so they can act in different ways. And that's actually quite powerful, because you can, theoretically, use these strategies to correct for different genetic rare conditions. So I think going to the sort of first part of your question, maybe if I can phrase it as "directly at source". If you can go upstream and target in a very direct way the cause of a rare condition, then actually you might be able to apply those same principles to many different types of rare condition. We know that there are, you know, 8,000 as a very ballpark number of rare conditions, and it might be that these strategies could be used I don't want to say for all rare conditions, but for many rare conditions where we find the genetic cause, these strategies could collectively be a very powerful way to treat them. And traditionally we've had to understand all the underlying biology, find a druggable target, find a drug that could target that, that's safe, effective, et cetera. And that's a lot of work. And that's still very, very valuable. If we were going to do this for these thousands of conditions, it would probably take us hundreds to thousands of years, collectively. And these strategies provide a lot of hope for being able to do this in a, in a more efficient way, where we can actually use the information used to treat one rare condition and apply those learnings to another rare condition. Sharon : I mean, that's really helpful to understand. So if the science is there, why aren't more patients benefiting from it yet? You know, what's standing in the way from your perspective? Ana Lisa: That's a really good question, and it's complex because the, our whole ecosystem is made up of, of many parts that go from finding a potential strategy that could help a rare condition to a patient benefiting from that. And I think one thing that maybe we haven't touched on yet is the fact that rare conditions can be really rare and affect a really small number of people individually, even though we know collectively they affect so many. You know, in the past it's been easier, if you're taking a condition that's common, that affects thousands of people, it's easier to see and to be sure whether your new medicine is actually working as you think it does and should, and having the benefits that you think. The, the sort of regulators have really clear guidance. We have lots of knowledge about how to assess treatments and have a randomised clinical trial, for example. How the reimbursement process may work in a public healthcare system. And when you, when you, when you sort of set down into the really rare, this is difficult for each stage of the journey. The transformation that's needed is a whole, system-wide transformation to be able to regulate in a scalable, equitable way, these therapies that could actually be an N of one treatment for one individual, that actually maybe one day another individual may also benefit, and sometimes even a group of individuals. It's not just the, the regulator, it's also how do you make it viable. So again, you have to make it scalable, equitable. And even to implement in the NHS down to this very "N equals one" level, and demonstrate that patients could benefit from these treatments, might require sort of fancier ways of assessing these treatments, whether it's statistics, other methodology and I think it's really the system-wide nature that makes this tricky, but is also a fantastic opportunity for, for collaboration, because that, that sort of end goal and benefits could be so, so great. Sharon: Yeah, absolutely. And I mean, Mel, for your side of things, it must sound, you know, quite frustrating where the people in the rare community to not see the support being made more readily available? Mel: Yeah, it is particularly difficult for patients and their families. I think in our case, when you're dealing with a neurodegenerative condition, time is of the essence. So when you know that the science is available or it's ready, but you don't have the systems in place to implement them to the patients so that they can access these much-needed therapies, it's worrying and frustrating. And also I see our children are affected with, with, you know, one of these N of few conditions that there's, you know, there's only 59 confirmed cases of DHDDS worldwide, and we've seen how the system firsthand doesn't fit ultra-rare patients. We can't, when we were looking at drug repurposing, we can't do a traditional clinical trial because we don't have the patient numbers and we don't have the funding. So a placebo-controlled trial just wouldn't be possible for us when there's only, I think, seven confirmed patients in the UK and, um, four that we're actually in, in, in touch with. So it does feel, I think, as Ana Lisa was saying, that we really need a system rethink, um, and refit so that it does start to accommodate these ultra-rare conditions, especially now as there's therapies which are showing huge benefit to patients. Sharon: And so with like all of these challenges, where are you seeing things shift and what does meaningful progress really look like for you? Mel: At the end of last year, the MHRA announced that they were rewriting the regulatory framework for rare conditions, and that fills us with lots of hope for the future. They're recognising that the traditional systems don't work for particularly ultra-rare conditions, and now that we do have these therapies in the pipeline, we, we want to get the patients to be able to access them. And we're also seeing innovation in how evidence is generated and measured. We witnessed this firsthand with our son as he was undergoing baseline tests for his ASO therapy. You know, the use of digital biomarkers, of real-world evidence, how they're increasingly being used for these N of one or N of few populations. And how the individual receiving the treatment becomes their own comparator. So you're not relying on these big natural history studies of the disease or placebo controls. It's you're looking specifically at that individual, getting a really strong baseline and then looking, once they're dosed with the medication, is that improving or stabilising symptoms? So I think this shift in focus is really meaningful for the ultra-rare community and also for them to be part of the decision-making process of what, what benefits do they want from a drug? Like what is meaningful to them? I think there's much more talk about the patients and how the, what will benefit them most. It's not necessarily what the scientists would think or research would think would most benefit, but what, what would make a meaningful difference to the patient? Sharon: I mean, that's good to know because it's kind of putting the person at the centre of, you know, this is what it's all about, isn't it? It's not just the science. We're trying to treat people and it's putting people, people first. Ana Lisa: Just to build on that, it's exactly that, that awareness that is, is growing, I think, that there are so many people affected by a rare condition and, and however rare your condition is, someone has a right to have hope and that the system should be able to cater for many rare conditions, you know, whether they're an ultra-rare or an actually almost common rare condition, everybody should have a hope that we should be able to find a treatment. And it's not a hopeless situation that it's, you know, never going to happen or be too difficult. It's quite powerful, hope. If you can solve for the truly individualised medicine, then you at the same time may also be helping everyone in-between a really common condition and a really rare condition, because right now the system works for common conditions. And if you can take it right down to the sort of radical of, example of an individualised medicine made for one person, then you are also forcing the system to a change for everybody else. And I think that's one of the great benefits of thinking about it as a joined-up system. Sharon: So how do you each navigate between hype versus hope when it comes to rare therapies? Mel? Mel: I like to focus on hope, because when we got our diagnosis, we felt really hopeless and that's a really dark place for a family to be. But as we learnt more about their condition and the rare condition landscape and genomics, we actually learned of all these new therapies that were in the pipeline. We were hearing about, you know, recently, conditions like Huntington's Disease that you never, never previously had any disease-modifying treatment, how they're now being able to be treated with gene therapy with really positive effects. Similarly for other neurodegenerative conditions that have been treated with ASOs, how they're seeing not just disease stabilisation, but improvements. So I know it's, it's still, like, relatively early days with these technologies and therapies, but I think it, it allows families to have hope, which is, which is really, really important, because that statistic, you know, of the, of 95% of rare conditions not having a treatment, it's, it's a really brutal one, uh, to be told at the outset or to learn at the outset. So, you know, if, if these therapies can, can make a huge dent in that, that would be life-changing. It would make a profound difference to many, many families, and I think there's a lot of reason to have hope, taking all of that into consideration. Sharon: And then Lisa? Ana Lisa: I think to work in this area, one needs to be full of hope and optimism because there are so many, um, challenges to overcome as a community. Uh, but I think that means that people are also incredibly collaborative, because they know that we need to work together for this to succeed. And no one, you know, one individual, one organisation can do it on their own. It truly has to be a crosscutting, collaborative endeavour. The fact that we, in the UK, have resources like the National Healthcare System,Genomics England in partnership with the NHS runs a National Genomic Research Library. And so the fact that you could look at, at tens of thousands of, of genomes for many, many individuals with rare conditions. That gives me hope because it means that if a treatment is made for another person, it could be in a different country in the world, and if we could find another patient, it doesn't matter what specialty they're under, where they are, we should be able to find them and connect with their clinical team if, you know, if they've consented for the National Genomic Research Library. And so to me, that feels, that whilst there's, there is a lot of hype in the sense that some of the really well-publicised cases, really had a lot of people working on them and a lot of resources to make it happen. But that gives hope to everybody else that follows that actually it is doable and if we can make better systems, and having these national resources that we do, the fact that, there are a lot of guidelines being written at the moment, both international and national. And again, they show that the sort of scaffolding is starting to be in place to apply these in an equitable scalable way. It might not be that you're so much looking for a specific rare condition as for a particular type of genetic variant that could be targeted in the same strategic way, and that therefore you could look across many different rare conditions. So again, all these sort of pieces of the puzzle are, are filling me with, with, with hope. Sharon: You touched upon, um, inequity there. Now, you know, is there a risk of inequity given what we've talked about in terms of those challenges? Ana Lisa: I think we, we always have to have the lens of equity in everything we, we do. And that, and that really does apply to healthcare and, and in fact, probably the whole rare disease community are, are, are not well served in terms of therapies at the moment. There are so few, um, therapeutic options and so I think there's a massive inequity in that this, our systems are not geared, uh, towards rare conditions. I suppose, you know, different countries have different healthcare systems and some of the sort of first personalised therapies may require a lot of money behind them to, to happen, but they will be pioneers in leading the way for how this can be done. And I think in the UK we have a lot of the infrastructure and the, a sort of a strong, that's very equitable, I think. And so we could do this in a, in a much more open and equitable way. Sharon: Mel? Mel: Cost is always, unfortunately, and it, when it's your family that's affected you, you know, you hate the thought that things are coming down to cost and, and money. But I, I think as Ana Lisa said, if, if the system absorbs the initial cost. You know, it seems that those longer-term costs could come down significantly. We already see with our very small DHDDS community that an ASO, which is an allele specific that was made personally for one, for one child, can actually also benefit my son, even though they have a different variant. So if the cost of the ASO is 1.2 million per person, but if you suddenly find actually one other person can share that, that's almost halving the, the cost. And then if then you're finding out that actually, oh no, 3, 4, 5, 10 people can all have that same ASO, suddenly it becomes much more cost-effective and more sustainable. So I think, as we have to think about cost, I think that also allows us to have more hope that these therapies can, the cost of these therapies that are obviously hugely expensive at the moment, can be brought down in the longer term. Ana Lisa: There are a lot of things that people want to do in the NHS. People can be working under quite hard circumstances, so to talk about making a therapy for one individual can be difficult and people can sometimes, I think, think that it's a pie-in-the-sky conversation. However, I think that, you know, all the clinicians I know who work with families with rare conditions, what they'd most like to be able to do is to be able to offer a therapy. And so I think a lot of people see this as a, as a big opportunity, despite these initial hurdles. One thing I often think about is my grandfather, when he was alive, every phone conversation, he would start with, "How many lives have you saved today?" And so I think that's the, that's our challenge. Sharon: Wow. That's, that's really powerful. Mel: Just echoing really what Ana Lisa was saying, I feel the, um, inequity lies in rare conditions as a, as a whole, from the point of diagnosis to the lack of pathway, um, to, to the lack of system in place for them. You wouldn't have a patient with a life-changing cancer diagnosis receive that information in a telephone call, and that is the stark reality for many rare disease patients. That's how they receive the, that's how they often receive the news. That was certainly our, our experience. And, and from that point, there was then no pathway. It's just this horrendous feeling of isolation. And I think now that there are these treatments in place and therapies in, in place, it's about time we change that because often the rare, the rare condition community, and certainly those with ultra-rare conditions as well, they're probably like some of the most underserved members of the community in that it's their parents and their families that have to advocate. Otherwise, without that, they, they often wouldn't stand a chance of understanding the disease, let alone finding a treatment. So I think the whole system needs to have a reset, to think about these rare condition patients and, put them at the heart as they do for more common conditions. Ana Lisa : I completely agree. And you mentioned cancer, and there are actually quite a few parallels. So there might be really common cancers that affect a lot of people that are being, uh, subsetted down into different groups depending on the genetics that are related to that particular cancer and therefore what treatments might be most effective. And so I think there's, there's a lot we can each learn from each other between the rare disease and cancer communities. Perhaps as in rare disease we scale up to apply the same strategies to many different rare conditions and patients. Even if they're being tweaked for their particular genetic variant and cancer, sometimes one is subsetting down to treat specifically that, exactly that cancer subtype. So there's a lot we can learn and I completely agree that the, the rare disease community deserves the same chance at at treatments, and the hope that that comes with. Sharon: Thank you. It feels like there needs to be some kind of seismic system change along with this piece around collaboration and how, you know, the science is there, but it's how do we bring it to families who are facing these difficulties with it, you know, their children and, and rare conditions. We'll wrap it up there. Thank you to our guests, Ana Lisa Tavares and Mel Dixon, for joining me as we discussed the evolving landscape of individualised medicines. And thank you for listening. If you'd like to hear more like this, please subscribe on your favorite podcast app. Behind the Genes is produced by Deanna Barac, Florence Cornish, Sophie McLachlan and Patrick Wallace at Bespoken Media.  

Ageing with HIV brings new challenges. Even with effective ART, people ageing with HIV face increased risk of parkinsonism. Eran F Shorer from the Icahn School of Medicine at Mount Sinai joins us to explore the latest research on brain changes, motor slowing, and the need for better diagnosis and treatment.https://www.thelancet.com/journals/lanhiv/article/PIIS2352-3018(25)00262-0/fulltextContinue this conversation on social!Follow us today at...https://thelancet.bsky.social/https://instagram.com/thelancetgrouphttps://facebook.com/thelancetmedicaljournalhttps://linkedIn.com/company/the-lancethttps://youtube.com/thelancettv

Join EEG legend Jay Gunkelman (500,000+ brain scans read) and host Pete Jansons for a deep dive into how montage selection changes what you see in brain maps — and why it matters for clinical accuracy.From LORETA source analysis to the newly validated male vs. female EEG differences, Jay breaks it all down with his signature "bad art" screen shares, landmark UCLA research, and real-world clinical insight.

Join EEG legend Jay Gunkelman (500,000+ brain scans read) and host Pete Jansons for a thorough exploration of Sensorimotor Rhythm (SMR) — the calming, stabilizing brainwave discovered by Barry Sterman.From cats trained on SMR that resisted toxic rocket fuel seizures (NASA origins) to modern uses in ADHD, epilepsy, insomnia, fibromyalgia, and arousal regulation — this episode breaks down the science, circuits, and clinical realities.✅ Key Topics Covered:Barry Sterman's breakthrough: SMR-trained cats survived rocket fuel doses that caused vomiting, panting, salivating, and seizures in controls (ruined the dose-response curve)Brain circuitry: Thalamus (ventroposterior lateral nucleus) + reticular nucleus (acetylcholine bursts) → sensory-motor cortex feedback → red nucleus quieting → muscle spindle relaxationSMR as daytime "sleep spindle": Stabilizes red nucleus (Parkinsonism target), cuts sympathetic drive, deeper muscle relaxation, reduces sensory feedback to thalamusBenefits: Epilepsy stabilization, fibromyalgia (quiets sympathetic input to red nucleus), ADHD clusters (excess theta/alpha, beta compensation), arousal-performance curve centeringRisks: Overtraining SMR drops arousal too far → underarousal/grogginess/rebound giddiness (like kids pre-bedtime); counter with anterior beta (17Hz functional beta on tasks)Arousal-performance: SMR = brakes (calms overarousal); beta = accelerator (fixes underarousal); no fixed sessions (10 for mild insomnia, 24+ for severe)ADHD insights: Frontal suppressor strip → caudate/putamen/globus pallidus/thalamus loop (excess GABA inhibition); beta magnitude increases (more events, not amplitude)

Listen Online: About this episode: In this thought-provoking conversation, Ann Louise Gittleman sits down with neurologist Dr. Thomas Guttuso, Jr., author of The Promise of Lithium, to explore the emerging role of carefully dosed lithium in neurodegenerative disease. Why is Parkinson's now the fastest-growing neurological disease? Dr. Guttuso explains what's driving the surge, how Parkinson's differs from Parkinsonism, and why men are diagnosed more often than women. He also introduces what he calls the brain's “Bermuda Triangle” — a vulnerable region tied to progressive neuron loss — and shares insight into a promising blood marker, neurofilament light (NFL), that may help track early damage. From there, the conversation turns to why dose and form are everything when it comes to lithium — and how the small amounts he uses clinically differ dramatically from the psychiatric doses most people associate with the mineral. He also addresses timing, prevention, L-Dopa, and whether early support could change the trajectory of these conditions. If you're concerned about Alzheimer's, Parkinson's, stroke, MS, or simply protecting long-term brain health, this interview offers a grounded and science-driven perspective on a mineral that may hold broader implications than many realize.  Check out Dr. Guttoso’s book at https://amzn.to/3YUgv4p and the form of lithium he recommends at https://amzn.to/4k7xDxE. The post The Promise of Lithium for Alzheimer's, Parkinson's and MS first appeared on Ann Louise Gittleman, PhD, CNS.

In this episode, host Ken Vinacco interviews Jessica Shurer, CurePSP's Director of Clinical Affairs and Advocacy, to share how the organization is leading initiatives to expand support, outreach, and education for individuals with PSP, MSA and CBS/CBD. The conversation highlights current advocacy efforts, the importance of early recognition, and the need for interdisciplinary collaboration. If you're interested in  elevating care for patients with atypical Parkinsonism, this episode is for you!  For questions about this podcast, please contact neuroddsig@gmail.com.  Show notes available here: https://app.box.com/s/o8b2u47sgoqnj133ky3d93cpo70ge7ab

We cover Parkinson's Disease, including pathophysiology, symptoms, causes and Parkinson's Disease treatment. PDFs available at: https://rhesusmedicine.com/pages/neurologyConsider subscribing (if you found any of the info useful!): https://www.youtube.com/channel/UCRks8wB6vgz0E7buP0L_5RQ?sub_confirmation=10:00 What is Parkinson's Disease? 0:30 Parkinson's Disease Pathophysiology 3:56 Parkinson's Disease Symptoms6:05 Parkinson's Disease Causes & Risk Factors7:18 Parkinson's Disease Diagnosis 8:47 Parkinson's Disease Treatment10:08 Parkinson's Disease On/Off Phenomenon ReferencesZafar, S. & Yaddanapudi, S.S. (2023). Parkinson Disease. Publishing. Available at: https://www.ncbi.nlm.nih.gov/books/NBK470193/Parkinson's Foundation. (2018). Statistics | Parkinson's Foundation.  Available at: https://www.parkinson.org/understanding-parkinsons/statistics Kenhub. (2023). Basal ganglia: Gross anatomy and function.  Available at: https://www.kenhub.com/en/library/anatomy/basal-gangliaBahners, B.H. et al. (2022). Electrophysiological characterization of the hyperdirect pathway and its functional relevance for subthalamic deep brain stimulation. Available at: https://www.sciencedirect.com/science/article/pii/S0014488622000565Ohio State University. (2017). Pathophysiology and Clinical Presentation | Parkinson's Disease Case Study. Available at: https://u.osu.edu/parkinsonsdisease/pathophysiology-and-clinical-presentation/ (U.OSU)Johns Hopkins Medicine. (n.d.). Parkinson's Disease Risk Factors and Causes.  Available at: https://www.hopkinsmedicine.org/health/conditions-and-diseases/parkinsons-disease(2024.). Parkinsonism vs. Parkinson's Disease: What's The Difference?.  Available at: https://parkinsonsdisease.net/answers/parkinsonism-vs-pdPostuma, R.B. et al. (2018). New Diagnostic Criteria for Parkinson's Disease: MDS-PD Criteria. Movement Disorders. Available at: https://pubmed.ncbi.nlm.nih.gov/29433115/(2018). MDS Clinical Diagnostic Criteria for Parkinson's Disease (PD). Available at: http://medicalcriteria.com/web/mds-parkinson-disease/(n.d.). Parkinson's Disease Side Effects of Medication. Available at: https://www.parkinsonsdaily.com/parkinsons-disease-side-effects-of-medication/(2020). Neuroscience Online: Chapter “Basal Ganglia”. Available at: https://nba.uth.tmc.edu/neuroscience/m/s3/chapter04.htmlDisclaimer: Please remember this podcast and all content from Rhesus Medicine is for educational and entertainment purposes only and is not a guide to diagnose or to treat any form of condition. The content is not to be used to guide clinical practice and is not medical advice. Please consult a healthcare professional for medical advice.

#Parkinsons #parkinonsdisease #parkinsonsawareness #LightTherapy #GutBrainConnection #SYMBYX #Photobiomodulation #ParkinsonsTreatment #ChronicIllnessHealing #Neurodegeneration In this powerful episode, we sit down with Dr. Wayne Markman, DC, the visionary co-founder and CEO of  @symbyxbiome  SYMBYX Biome — an Australian MedTech company pioneering non-invasive, light-based therapies for Parkinson's disease. A Harvard MBA and Doctor of Chiropractic, Dr. Markman brings both personal passion and clinical expertise to his mission of improving quality of life for those living with Parkinson's. SYMBYX is leading global research into the gut-brain connection and the use of photobiomodulation (light therapy) as a groundbreaking treatment approach. We explore: -Why the gut-brain axis could be the key to treating Parkinson's -How SYMBYX lasers are used to target inflammation and improve symptoms -The current state of global clinical trials and regulatory approvals -What's next for light therapy and neurodegenerative conditions If you're curious about non-pharmaceutical, evidence-backed ways to manage Parkinson's—or you want a front-row seat to the future of personalized medicine—this episode is for you.

Could a natural compound from everyday spices protect your brain and slow the progression of Parkinson's Disease? In this episode (watch on YouTube here!) you will learn about β-caryophyllene (BCP)—a safe, plant-derived compound found in black pepper, rosemary, and hops. BCP is FDA- and EFSA-approved as a flavor enhancer, but research suggests it does far more. What you'll learn in this episode: ✅ How BCP protects dopamine neurons in the substantia nigra ✅ Its potential role in stabilizing Parkinson's and slowing progression  ✅ Symptom relief for pain, restless legs, muscle hesitation, depression, anxiety, and sleep issues ✅ How BCP may treat tardive dyskinesia caused by medications ✅ BCP's broader neuroprotective, anti-inflammatory, and antioxidant properties Whether you're living with Parkinson's, caring for someone who is, or interested in natural neuroprotection, this episode will expand your understanding of what's possible. Be sure to explore the BCP products that you heard about in this episode that are available from Blair Medical Group via this link (Enter promo code PDEDUCATION for a 10% discount on your order): https://www.blairmedicalgroup.shop/shop/bcplus-endocannabinoid-activation-products/2?aff=22

Parkinsonism is the term used to refer to a group of conditions – like multiple system atrophy (MSA), progressive supranuclear palsy (PSP), corticobasal degeneration (CBD) and Lewy Body Dementia – which resemble Parkinson's in some of their symptoms. To discuss these sibling conditions, the Movers & Shakers are joined at the pub by guests from across the spectrum who share their stories – often very uplifting – about learning to live with the new realities brought on by their illnesses.Sponsored by Albion Chambers.Presented by Rory Cellan-Jones, Gillian Lacey-Solymar, Mark Mardell, Paul Mayhew-Archer, Sir Nicholas Mostyn and Jeremy Paxman.Produced and edited by Nick Hilton for Podot.Sound mixing by Ewan Cameron.Music by Alex Stobbs. Hosted on Acast. See acast.com/privacy for more information.

Delaying diagnosis of parkinsonism can mean delaying care. In a study recently published in JAMA Neurology, David Vaillancourt, PhD, and colleagues tested the ability of an AI model to differentiate between Parkinson disease and other neurodegenerative disorders when paired with MRI. He joins JAMA and JAMA+ AI Associate Editor Yulin Hswen, ScD, MPH to discuss. Related Content: A Large Proportion of Parkinson Disease Diagnoses Are Wrong—Here's How AI Could Help Automated Imaging Differentiation for Parkinsonism

Could eating only meat actually help with Parkinson's Disease? In this episode (watch on YouTube), we explore the controversial and compelling carnivore diet—a 100% animal-based approach—and why some people with Parkinson's are turning to it for inflammation reduction, gut healing, and brain support. We cover: -How the carnivore diet may reduce neuro-inflammation -Why ketosis could be protective for dopamine-producing neurons -The connection between oxidative stress and Parkinson's progression -How ketones support cellular cleanup (autophagy) and mitochondrial function -Nutrients in animal-based diets that support brain and nerve health -Risks, cautions, and who this diet may NOT be right for Whether you're carnivore-curious or just exploring ways to optimize your Parkinson's care naturally, this episode dives into the “why” behind the trend. Be sure to enhance ketosis among other benefits with Dr. Blair's Beta-Caryophyllene products here (Use promo code PDEDUCATION at checkout to save 10%!!): https://www.blairmedicalgroup.shop/shop/bcplus-endocannabinoid-activation-products/2?aff=22 Learn how to use carnivore to help manage Parkinson's by exploring this course https://pdeducation.thinkific.com/products/courses/empowerhealing JUMPSTART protocol here: https://pdeducation.thinkific.com/products/digital_downloads/30dayjumpstart 

Progressive supranuclear palsy and corticobasal syndrome are closely related neurodegenerative disorders that present with progressive parkinsonism and multiple other features that overlap clinically and neuropathologically. Early recognition is critical to provide appropriate treatment and supportive care. In this episode, Teshamae Monteith, MD, FAAN speaks with Nikolaus R. McFarland, MD, PhD, FAAN, author of the article “Progressive Supranuclear Palsy and Corticobasal Syndrome” in the Continuum® August 2025 Movement Disorders issue. Dr. Monteith is the associate editor of Continuum® Audio and an associate professor of clinical neurology at the University of Miami Miller School of Medicine in Miami, Florida. Dr. McFarland is an associate professor of neurology at the University of Florida College of Medicine at the Norman Fixel Institute for Neurological Diseases in Gainesville, Florida. Additional Resources  Read the article: Progressive Supranuclear Palsy and Corticobasal Syndrome Subscribe to Continuum®: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @headacheMD Full episode transcript available here Dr Jones: This is Dr Lyell Jones, Editor-in-Chief of Continuum. Thank you for listening to Continuum Audio. Be sure to visit the links in the episode notes for information about earning CME, subscribing to the journal, and exclusive access to interviews not featured on the podcast. Dr Monteith: Hi, this is Dr Teshamae Monteith. Today I'm interviewing Dr Nikolaus McFarland about his article on progressive supranuclear palsy and cortical basilar syndrome, which appears in the August 2025 Continuum issue on movement disorders. Welcome, how are you? Dr Farland: I'm great. Thank you for inviting me to do this. This is a great opportunity. I had fun putting this article together, and it's part of my passion. Dr Monteith: Yes, I know that. You sit on the board with me in the Florida Society of Neurology and I've seen your lectures. You're very passionate about this. And so why don't you first start off with introducing yourself, and then tell us just a little bit about what got you interested in this field. Dr Farland: I'm Dr Nicholas McFarlane. I'm an associate professor at the University of Florida, and I work at the Norman Fixel Institute for Neurological Diseases. I am a director of a number of different centers. So, I actually direct the cure PSP Center of Care and the MSA Center of Excellence at the University of Florida; I also direct the Huntington's clinic there as well. But for many years my focus has been on atypical parkinsonisms. And, you know, I've treated these patients for years, and one of my focuses is actually these patients who suffer from progressive supranuclear palsy and corticobasal syndrome. So that's kind of what this review is all about. Dr Monteith: You probably were born excited, but I want to know what got you interested in this in particular? Dr Farland: So, what got me interested in this in particular was really the disease and the challenges that's involved in it. So, Parkinson's disease is pretty common, and we see a lot of that in our clinic. Yet many times, roughly about 10 to 15% of my patients present with these atypical disorders. And they're quite fascinating. They present in different ways. They're fairly uncommon. They're complex disorders that progress fairly rapidly, and they have multiple different features. They're sort of exciting to see clinically as a neurologist. I think they're really interesting from an academic standpoint, but also in the standpoint of really trying to bring together sort of a team. We have built a multidisciplinary team here at the University of Florida to take care of these patients. They require a number of folks on that team to take care of them. And so, what's exciting, really, is the challenge of treating these patients. There are very limited numbers of therapies that are available, and the current therapies that we have often really aren't great and over time they fail. And so, part of the challenge is actually doing research. And so, there's actually a lot of new research that's been going on in this field. Recently, there's been some revisions to the clinical criteria to help diagnose these disorders. So, that's really what's exciting. The field is really moving forward fairly rapidly with a number of new diagnostics, therapeutics coming out. And hopefully we can make a real difference for these patients. And so that's what really got me into this field, the challenge of trying to treat these patients, help them, advocate for them and make them better. Dr Monteith: And so, tell me what the essential points of this article. Dr Farland: So, the essential points, really, of this article is: number one, you know, just to recognize the new clinical criteria for both PSP and corticobasal syndrome, the diagnosis for these disorders or the phenotypic spectrum has really expanded over the years. So, we now recognize many different phenotypes of these disorders, and the diagnosis has gotten fairly complicated. And so, one of the goals of this article was to review those new diagnostic criteria and the different phenotypic ways these diseases present. I wanted to discuss, also, some of the neuropathology and clinicopathological overlap that's occurred in these diseases as well as some of the new diagnostic tests that are available. That's definitely growing. Some of the new studies that are out, in terms of research and clinical trials. And then wanted to review some of the approaches for treatment for neurologists. Particularly, we're hoping that, you know, this article educates folks. If you're a general neurologist, we're hoping that recognizing these diseases early on will prompt you to refer these patients to specialty clinics or movement disorder specialists early on so they can get appropriate care, confirm your diagnosis, as well as get them involved in trials if they are available. Dr Monteith: And how has the clinical criteria for PSP and cortical basilar syndrome changed? Dr Farland: I think I already mentioned there's been an evolution of the clinical criteria for PSP. There's new diagnostic criteria that were recently published, and it recognizes the multiple clinical phenotypes and the spectrum of the disease that's out there, which is much broader than we thought about. Corticobasal clinical criteria are the Dr Armstrong criteria from 2013. They have not been updated, but they are in the works of being updated. But it does recognize the classic presentation of corticobasal syndrome, plus a frontal executive predominant and then a variant that actually overlaps with PSP. So, there's a lot more overlap in these two diseases than we originally recognized. Dr Monteith: And so, you spoke a bit about FTD spectrum. So why don't you tell us a little bit about what that is? I know you mentioned multiple phenotypes. Dr Farland: What I really want to say is that both PSP and corticobasal syndrome, they're relatively rare, and what- sort of as to common features, they both are progressive Parkinson disorders, but they have variable features. While they're commonly associated with Parkinson's, they also fit within this frontotemporal lobar spectrum, having features that overlap both clinically and neuropathologically. I just want folks to understand that overlap. One of this pathological overlap here is the predominant Tau pathology in the brain, an increasing recognology- recognition of sort of the pathological heterogeneity within these disorders. So, there's an initial description, a classic of PSP, as Richardson syndrome. But now we recognize there are lots of different features to it and there are different ways it presents, and there's definitely a lot of clinical pathological overlap. Dr Monteith: Why don't we just talk about some red flags for PSP? Dr Farland: Yeah, sure. So, some of the red flags for PSP and even corticobasal syndrome are: number one is rapid progression with early onset of falls, gait difficulty, falling typically backwards, early speech and swallow problems that are more prominent than you see in Parkinson's disease, as well as eye gaze issues. So, ocular motor features, particularly vertical gaze palsy. In particular what we talk about is the supranuclear gaze palsy, and one of the most sensitive features that we've seen with these is downgaze limitation or slowed downgaze, and eventually a full vertical gaze palsy and followed supranuclear gaze palsy. So, there's some of the red flags that we see. So, while we think about the lack of response to levodopa frequently as something that's a red flag for Parkinson's, there are many times that we see Parkinson's patients, and about a quarter of them don't really respond. There's some features that don't respond to levodopa that may not be so specific, but also can be helpful in this disease. Dr Monteith: And what about the red flags for cortical basilar syndrome? Dr Farland: So, for cortical basilar syndrome, some of the red flags again are this rapidly depressive syndrome tends to be, at least in its classical present presentation, more asymmetric in its presentation of parkinsonism, with features including things like dystonic features, okay? For limb dystonia and apraxias---so, inability to do a learned behavior. One of those red flags is a patient who comes in and says, my hand doesn't work anymore, which is something extremely uncommon that you hear in Parkinson's disease. Most of those patients will present, say, I might have a tremor, but they very rarely will tell you that I can't use my hand. So look out for that sign. Dr Monteith: And let's talk a little bit about some of the advances in the fields you mentioned, evolving biomarker and imaging capacities. So, how are these advances useful in helping us understand these conditions, especially when there's so much heterogeneity? Dr Farland: I might start by talking a little bit about some of the clinical criteria that have advanced. Why don't we start there and just discuss some of the advances? I think in PSP, I think, originally we had both probable and possible diagnoses of PSP, and the diagnostic criteria were basically focused on what was what's called “classical PSP” or “Richardson syndrome”. But now we recognize that there are multiple phenotypes. There's an overlap with Parkinsonism that's slower in progression and morphs into PSP, the classical form. There's a frontal behavioral variant where patients present with that frontal behavioral kind of thing. There's a speech-language variant that can overlap with PSP. So they have prominent speech language, potentially even apraxia speech. So, recognition of these different phenotypes is sort of a new thing in this field. There's even overlap with cortical basal syndrome and PSP, and we note that the pathology can overlap as well. So, I think that's one of the things that have changed over time. And these were- recently came out in 2017 in a new publication in the Movement Disorders Society. So, in terms of diagnostic tests as well---and there's been quite a bit of evolution---really still to date, our best diagnostic test is imaging. MRI is really one of our best tests currently. Currently blood tests, spinal fluid, there's new biomarkers in terms of skin… they're still in the research phase and not necessarily very specific yet. So, we rely heavily on imaging still; and for PSP, what we're looking for largely are changes in the brain stem, and particularly focused on the midbrain. So disproportionate midbrain atrophy compared to the pons and the rest of the midbrain is a fairly specific intensive sign for PSP. Whereas in MSA we see more of a pontine atrophy compared to the midbrain. So that can be really helpful, and there are lots of different new measurements that can be done. PET scans are also being used as well. And there are new PET markers, but they still remain kind of research-based, but are becoming more and more prevalent and may be available soon for potential use. Although there's some overlap with PET tracers with Alzheimer's disease and different Tau isoforms. So, something to be wary about, but we will be seeing some of these soon coming out as well. More kind of up-to-date things include things like the spinal fluid as well as even some of the skin biopsies. And I think we've heard some word of recent studies that have come out that potentially in the very near future we might actually have some Tau protein tests that we can look at Tau either in spinal fluid or even in a skin biopsy. But again, still remains research-based and, we still need more information as to whether these tests can be reproducible and how sensitive or specific they are. Dr Monteith: It sounds like, when really approaching these patients, still, it's a lot of back to the history, back to the clinical and some basic imaging that we should be able to identify to distinguish these types of patients, and we're not quite where we need to be yet for biomarker. Dr Farland: I totally agree with you. I think it starts, really, with the clinical exam and that's our main focus here; and understanding some of the new clinical criteria which are more sensitive, but also specific, too. And they're really useful to look at. So, I think reviewing those; patients do progress, following them over time can be really useful. And then for diagnosis, getting imaging if you suspect a patient has an atypical presentation of parkinsonism, to look for signs or features that might be specific for these different disorders. Dr Monteith: Why don't we take a typical case, a typical patient that you would see in clinic, and walk us through the thought process---especially, maybe they presented somewhat early---and the different treatment approaches to helping the patient, and of course their family. Dr Farland: Yeah, sure. So, a typical patient might be someone who comes in with, like, a three year history of progressive gait problems and falling. And let's say the patient says, I'm falling backwards frequently. They may have had, like, a rib fracture, or they hit their head once, and they're describing some speech issues as well. Now they're relying on a walker and family members saying they rarely let them be by themselves. And there may be some slowing of their cognitive function and maybe a bit of withdrawal. So that's a typical patient. So, the approach here is really, what are some of the red flags? I think already you hear a red flag of a rapidly progressive disease. So, Parkinson's disease patients rarely have frequent falls within the first five years. So, this is within three years or less. You're already hearing early onset of gait problems and falling, and particularly falling backwards rather than forwards as often Parkinson's disease patients do. You're hearing early speech problems and maybe a subtle hint of cognitive slowing and some withdrawal. So, a lot of things that sort of are red flags. So, our approach really would be examining this patient really closely. Okay? We'd be listening to the history, looking at the patient. One thing is that some of these patients come in, they may be in a wheelchair already. That's a red flag for us. If they're wearing sunglasses---sometimes we see that patients, they have photosensitivity and they're in a chair and they're wearing sunglasses---you take the glasses off and you look at their face and they have that sort of a facial stare to them---not just the masked face, but the stare---and their eyes really aren't moving. So, another kind of clue, maybe this is probably something atypical, particularly PSP is what I'm thinking about. So, the approach is really, do a thorough exam. I always recommend looking at eye movements and starting with volitional saccades, not giving them a target necessarily, but asking them to look up and then look down. And then particularly look at the speed of downgaze and whether they actually have full versions down, are able to do that. That's probably your most sensitive test for a patient who has PSP. Not the upgaze, which can be- upgaze impairment in older patients can be nonspecific. So, look for that down gaze. So, if I can get out one message, that's one thing that can be easily done and examined fairly quickly for diagnosis of these patients. And then just look for signs of rigidity, bradykinesia, maybe even some myelopraxia, and then look at their gait carefully so that there's a high suspicion. Again, if there's some atypical features, imaging is really important. So, my next step would be probably getting an MRI to evaluate whether- do they have brain somatrophy or other widespread atrophy or other signs? You need to think about your differential diagnosis for some of these patients as well. So, common things are common; vascular disease, you can't have vascular parkinsonism or even signs of NPH. Both of those can present with progressive gait difficulty and falls. So, the gait may look more like Parkinson's rather than ataxic gait that we see in classic PSP, but still they have early gait issues, and that can be a mimicker of PSP, So looking for both of those things in your imaging. Think about sort of autoimmune potentially causes. So, if they have a really rapid progressive cause, there are some rare autoimmune things. There have been recent reports of things like IgLON5, although there's limited cases, but we're doing more screening for some of those autoimmune causes. And then even some infectious causes like Whipples, that are rarely present like this. Okay? And have other signs and features. Dr Monteith: So, let's say you diagnose this patient with PSP and you're assessing the patients to see how you can improve their quality of life. So, what are some potential symptomatic managements that will help our patient? Dr Farland: I recommend for most all of these patients… while the literature indicates that many patients with PSP, and especially corticobasal syndrome, don't respond well to levodopa. So, the classic treatment for parkinsonism. However, we all recommend a trial of levodopa. These patients may respond partially to doses of levodopa, and we try to push the doses a bit higher. So, the recommended trial is usually a dose up to roughly 1000 milligrams of levodopa per day. And give it some time, at least two, if not actually three months of a trial. If not well-tolerated, you can back off. If there's no response at all or no improvement, then slowly back off and taper patients off and ask them to tell you whether they feel like they're actually worsening. So, many patients, sometimes, don't recognize the improvements, or family members don't recognize it until we actually taper them back off. And they may end up saying there are some other things that even recognize. Even some nonmotor benefits can be seen with levodopa. In some cases, we do keep them on levodopa, but levodopa's our best therapy for this. Dopamine agonists, MAO inhibitors, have all been sort of tried and they've been studied, but often don't really help or fail to help benefit these patients and could be fraught with some other side effects. I think many people do also turn to Amantadine as a treatment for Parkinson's, gait problems, freezing, if you see it in these disorders. Yet Amantadine is fraught with issues of side effects, including cognitive issues, and I think is not well-tolerated. But there are the rare patient who actually does respond to this or claims they respond to this. By and large, these patients relentlessly progress, unfortunately. So, beside treatment of other symptoms, I think it's really important to recognize that they require supportive cares and therapy. So, starting those early on and getting your allied healthcares kind of involved. So that includes people like physical, occupational therapy for the gait issues, the falls, occupational therapy for doing daily activities. Speech language pathology can be really a critical player for these because of the early speech and language issues, as well as swallow difficulties. Swallow is compared quickly in these patients. And so, we do recommend the screening evaluation, then often following patients either every six- or even annually, at least, with a swallow evaluation. And we recommend the fluoroscopic-guided kind of modified barium swallow for these patients.  Dr Monteith: And how does that differ if, let's say, the patient had cortical basilar syndrome? What are some of the symptomatic treatments that would be high on your consideration? Dr Farland: So actually, these patients also have a very similar approach, and they often have some overlapping features. Maybe a little bit of difference in terms of the level of apraxia and some dystonic features that you see in corticobasal syndrome. So, as I mentioned earlier that these patients have a more typ- when they present, typically have a more asymmetric presentation. And one of the biggest issues is this limb apraxia. They may have abnormal movements as well as, like, the alien limb-type phenomena as well. So, the focus of therapy, while similar in the sense we focus on the parkinsonism, I do always try levodopa and try to ramp up the doses to see if it benefits. It does often fail, but it's definitely worth trying. The other focus of these patients is trying to treat symptoms. Dystonia, those features… in some cases, we can help; if it's painful or uncomfortable, muscle relaxants can be used. If it's vocal, things like Botox can be really helpful. Often times it is more palliative than actually restorative in terms of function, but still can be really helpful for patients who ask about pain and discomfort and trying to treat. And then of course, again, the focus on our supportive care. We need to build that network and build that team of folks, the therapists, the physical, occupational, and the speech therapist to help them. If they have language problems---like either in PSP or corticobasal---I'll also include my request to a speech language pathologist to work on cognitive function. That's a special, additional thing you have to ask for and then specifically request when you make a referral to a speech language pathologist. Dr Monteith: That is so important. I think keeping the simulation, keeping the social support, and I would probably guess that you would also include screening for sleep and mood disorder. Dr Farland: Absolutely. Mood disorders are really big in these diseases. Patients are suffering terribly. You do hear about labile mood in both of these diseases, particularly PSP; and even what's called pseudobulbar palsy, where the mood is not always congruent with the affect. So they may laugh or cry inappropriately, and particularly the crying can be very disturbing to family and caregivers to see that. And so, treating those things can be really important. So always asking about the mood issues. Depression in particular is something that we're very sensitive about, and there is a higher incidence of suicidal ideations. Asking about that and feeling and making sure that they are in a safe environment can be really important. Dr Monteith: Thank you so much. Dr Farland: Thank you. Dr Monteith: Today I've been interviewing Dr Nikolaus McFarland about his article on progressive supranuclear palsy and cortical basilar syndrome, which appears in the August 2025 Continuum issue on movement disorders. Be sure to check out Continuum Audio episodes from this and other issues, and thank you to our listeners for joining today. Dr Monteith: This is Dr Teshamae Monteith, Associate Editor of Continuum Audio. If you've enjoyed this episode, you'll love the journal, which is full of in-depth and clinically relevant information important for neurology practitioners. Use the link in the episode notes to learn more and subscribe. AAN members, you can get CME for listening to this interview by completing the evaluation at continpub.com/audioCME. Thank you for listening to Continuum Audio.

On this episode of Fishing the DMV, I'm joined by Dave Miller to dive into one of the most heated conservation debates facing our waters today overspray of herbicides in our local bodies of water. We tackle a hot-button issue shaking up the fishing and conservation community: The decision to use diquat dibromide—a federally approved herbicide that's banned in the European Union—to combat the spread of subaquatic grass has sparked serious concerns. Critics warn it is creating ecological disasters, killing fish in lakes, making people sick, and even causing the deaths of pets.A recent opinion piece slammed the move as reckless and undemocratic, arguing that spraying chemicals into public waterways risks fish kills, long-term ecological damage, and public health concerns. Critics point out the decision was made quietly by federal and state agencies, without town halls, public consent, or community input, raising serious questions about accountability.Even more concerning, this is part of a pilot program that could expand to other states if considered successful—potentially setting a precedent for how invasive species are managed nationwide. Meanwhile, alternatives such as mechanical removal and less toxic treatments have largely been overlooked. Parkinsonism relating to intoxication with glyphosate: a case Report: https://www.researchgate.net/publication/331317400_Parkinsonism_relating_to_intoxication_with_glyphosate_A_case_report Glyphosate Exposure Associated with Human Neurodegenerative Disorders: A Scoping Review: https://www.scirp.org/pdf/jbbs2024147_13901129.pdf  Dave Miller on Instagram: https://www.instagram.com/davemillerfishing/  Dave Miller website: https://l.instagram.com/?u=https%3A%2F%2Fdavemillerfishing.com%2F%3Ffbclid%3DPAZXh0bgNhZW0CMTEAAac_PqZE74JW2U5Z9QT-9AYXPlXuE6r27JeCwxi9v9kmocBrI4uey8nBtxt3zg_aem_hNSsX_SsybYNLI_1YxKSxA&e=AT1zGSItFBqz8Z_S0JFJAevn7rC_vd2PhDiWQrjiVx7CpMcHulAEHn1oCSl1zURX5EqR3B3COPIDXQGGRKM5Xcl5xD2A0qlIGwBbng  Please support Fishing the DMV on Patreon!!! https://patreon.com/FishingtheDMVPodcast  Fishing the DMV now has a website: https://www.fishingthedmv.com/ If you are interested in being on the show or a sponsorship opportunity, please reach out to me at fishingtheDMV@gmail.com Please checkout our Patreon Sponsors Catoctin Creek Custom Rods: https://www.facebook.com/CatoctinCreekCustomRods Jake's bait & Tackle website:                      http://www.jakesbaitandtackle.com/ Tiger Crankbaits on Facebook!! https://www.facebook.com/tigercrankbaits Jake's bait & Tackle website:                      http://www.jakesbaitandtackle.com/  Fishing the DMV Facebook page: Support the show

Parkinson's disease is rising faster than ever before — with 90,000 new U.S. cases every year. But what if it's not just bad luck, aging, or genetics? In this powerful conversation (watch HERE on YouTube), one of the world's leading neurologists, Dr. Michael Okun, reveals shocking truths from the new book The Parkinson's PLAN, co-authored with Dr. Ray Dorsey:  ☠️ The hidden toxins in our air, water, and food that are driving the disease

Parkinson disease is a neurodegenerative movement disorder that is increasing in prevalence as the population ages. The symptoms and rate of progression are clinically heterogenous, and medical management is focused on the individual needs of the patient. In this episode, Kait Nevel MD, speaks with Ashley Rawls, MD, MS, author of the article “Parkinson Disease” in the Continuum® August 2025 Movement Disorders issue. Dr. Nevel is a Continuum® Audio interviewer and a neurologist and neuro-oncologist at Indiana University School of Medicine in Indianapolis, Indiana. Dr. Rawls is an assistant professor at the University of Florida Health, Department of Neurology at the Norman Fixel Institute for Neurological Diseases in Gainesville, Florida Additional Resources Read the article:  Parkinson Disease Subscribe to Continuum®: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @IUneurodocmom Guest: @DrRawlsMoveMD Full episode transcript available here Dr Jones: This is Dr Lyell Jones, Editor-in-Chief of Continuum. Thank you for listening to Continuum Audio. Be sure to visit the links in the episode notes for information about earning CME, subscribing to the journal, and exclusive access to interviews not featured on the podcast. Dr Nevel: Hello, this is Dr Kait Nevel. Today I'm interviewing Dr Ashley Rawls about her article on Parkinson disease, which appears in the August 2025 Continuum issue on movement disorders. Ashley, welcome to the podcast, and please introduce yourself to the audience. Dr Rawls: Thank you, Kait. Hello everyone, my name is Dr Ashley Rawls. I am a movement disorder specialist at the University of Florida Fixel Institute for Neurologic Diseases in Gainesville, Florida. It's a pleasure to be here. Dr Nevel: Awesome. To start us off talking about your article, can you share what you think is the most important takeaway for the practicing neurologist? Dr Rawls: Yes. I would say that my most important takeaway for this article is that Parkinson disease remains a clinical diagnosis. I think the field has really been advancing and trying to find a biomarker to help with diagnosis through ancillary testing. For example, with the dopamine transporter, the DAT scan, an alpha-synuclein skin biopsy, an alpha-synuclein amplification assay that can happen in blood and CSF. However, I think it's so critical to make sure that you have a very strong history and a very thorough physical exam and use those biomarkers or other testing to help with, kind of, bolstering your thoughts on what's going on with the patient. Dr Nevel: Great. And I can't wait to talk a little bit more about the ancillary testing and how you use that. Before we get to that, can you review with us some of the components of the clinical diagnosis of Parkinson disease? Dr Rawls: Yes. So, when I think about a person that comes in that might have a neurodegenerative disease, I think about two different features, mainly: both motor and Manon motor. So, for my motor features, I'm thinking about resting tremor, bradykinesia---which is fullness of movement with decrement over time---rigidity, and then a specific gait disturbance, a Parkinsonian gait, involving stooped posture, decreased arm swing. They can also have reemergent tremor while walking if they do have tremor as part of their disease process, and also in-block turning as they are walking down the hallway. So, those are my motor features that I look for. So now, when we're talking about a specific diagnosis of Parkinson disease, the one motor feature that you need to have is bradykinesia. The reason why I make sure to speak about bradykinesia, which is slowness of movement with decrement over time, is because people can still have Parkinson disease without having tremor, a resting tremor. So even though that's one of the core cardinal features that most of us will be able to notice very readily, you don't have to necessarily have a resting tremor to be diagnosed with Parkinson' disease. When I talk about nonmotor features, those are going to be the three, particularly the prodromal features that can occur even ten years before people have motor features, can be very prominent early on in the disease process. For example, hyposmia or anosmia for decrease or lack of sense of smell. Another one that we really look for is going to be RBD, or rapid eye movement behavior disorder; or REM behavior disorder, the person acting out their dreams, calling out, flailing their limbs, hitting their bed partner. And then the other one is going to be severe constipation. So those three prodromal nonmotor symptoms of hyposmia/anosmia, RBD or REM behavior disorder, and severe constipation can also make me concerned as a red flag that there is a sort of neurodegenerative issue like a Parkinson disease that may be going on with the patient. Dr Nevel: Great, thank you so much for that overview. While we're talking about the diagnosis, do you mind kind of going back to what you mentioned in the beginning and talking about the ancillary tests that sometimes are used to kind of help, again, bolster that diagnosis of Parkinson disease? You know, like the DAT or the alpha-synuclein skin biopsy. When should we be using those? Should we be getting these on everyone? And what scenarios should we really consider doing one of those tests? Dr Rawls: The scenario in which I would order one of the ancillary testing, particularly like a DAT scan or a skin biopsy, looking for alpha-synuclein is going to be when there are potential red flags or a little bit of confusion in regard to the history and physical that I need to have a little bit more clarification on. For example, if I have a patient that has a history of using dopamine blocking agents, for example, for severe depression; or they have a history of cancer diagnosis and they've been on a dopamine agent like metoclopramide; those I want to be mindful because if they're coming in to see me and they're having the symptoms of Parkinsonism---which is going to be resting tremor, bradykinesia rigidity, or gait disturbance---I need to try to figure out is it potentially due to a medication effect, particularly if they're still on the dopamine blockade medication, or is it something where they're actually having a neurodegenerative illness underneath it, like a Parkinson disease? The other situation that would make me order a DAT skin or a skin biopsy is going to be someone who is coming in that maybe has elements of essential tremor, they have more of a postural or an intention tremor that's very flapping and larger amplitude, and maybe have some mild symptoms and Parkinsonism that might be difficult to distinguish between other musculoskeletal things like arthritis, other imbalance issues from, you know, hip problems or knee problems and what have you. Then I might say, okay, let's see if there is some sort of neurodegeneration underneath this; that may be- that there could be, you know, potentially two elements like a central tremor and Parkinson disease going on. Or is this someone who actually really has Parkinson disease, but there's other factors that are kind of playing into that. Dr Nevel: Great, thank you for that. Gosh, things have really changed over the past fifteen years or so where we have this ancillary testing that we're able to use more, because what you read in the textbook isn't always what you see in clinic. And as you described, there are patients who… it's not as clear cut, and these tests can be helpful. Could you tell us more about the levodopa challenge test? How is this useful in clinical practice? And what are some key points that we should know about when utilizing this strategy for patients who we think have Parkinson disease? Dr Rawls: So, before we had all this ancillary testing with the DAT scan, the skin biopsy, the alpha-synuclein amplification assay, many times if you had a suspicion that a person that had Parkinson disease, but you weren't entirely sure, you would say, hey, listen, let us give you back the dopamine that your body may be missing and see if you have an improvement, in particular in your motor symptom. So, when I talk with my patients, I say, listen, I might have a strong suspicion that you have Parkinson disease. Doing a levodopa trial can not only be diagnostic, but also can be therapeutic as well. So, with this levodopa trial, what I end up doing is saying, okay, we're going to start the medication at a low dose because we are looking to see if you have improvement in three of the main cardinal motor symptoms. Obviously, tremor is much easier for us to see if it gets better. It's very obvious on exam, and the patients are more readily able to see it. Whereas stiffness and slowness is much harder to quantify and try to figure out. Am I stiff and slow because of potential muscle tightness from Parkinson disease, or is it something that's more of a musculoskeletal issue? So, I will tell persons, okay, we're looking for improvement in these three cardinal motor symptoms, and things that we're looking for is getting into and out of a car, into and out of a chair, turning over in bed, seeing how do we navigate ourselves in our daily lives? I give people the example of going through the grocery store, going through a busy airport. Are we able to move better and respond better to different changes in our environment which can give us a better clue of if our stiffness and slowness in particular are being improved with the medication? The other part of this is talking about potential side effects of the carbidopa- of the levodopa in particular. One big thing that I think limits people initially is going to be the nausea, vomiting, potential GI upset when starting this medication initially. So, oftentimes I will find people coming in, oh, you know, my outside doctor started me immediately on one tab of carbidopa/levodopa three times per day. I got nauseous, I threw up, and I never took the medication again. So often times I will start low and go slow because once someone throws up my medication, they are not going to want to take it again---with good reason. So, often times I will ask the patient, hey listen, are you very sensitive to medications? If you are very sensitive, we might start one tablet per day for a week, one tablet twice a day, and then go up until we get to two tablets three times a day if we're talking about carbidopa/levodopa. If someone is not as sensitive then I might go up a little bit quicker. What do we mean when we talk about 600 milligrams per day? So usually, the amount that I use is carbidopa/levodopa, 25/100; so, 100 milligrams being the levodopa portion. Many people just start off at 1 tab 3 times a day, which gives you 300 milligrams of levodopa, and they say, oh, it didn't work, I must not have Parkinson or something else. Well, it just may have been that we did not give an adequate trial and adequate dose to the person. Now if they're not able to tolerate the medication because of the side effects, that's something different. But if they don't have side effects and don't notice a difference, there is room to increase the carbidopa/levodopa or the levodopa replacement that you are using so that you can give it, you know, a very good try to see, is it actually improving resting tremor, bradykinesia and rigidity? Dr Nevel: Yeah, great. Thanks for that. When you diagnose a patient with Parkinson disease, how do you counsel that patient? How do you break that difficult news? And how do you counsel them on what to expect in the future and goals of treatment? I know that's a lot in that question, but it also is a lot that you do in one visit, oftentimes, or at least introduce these kind of concepts to patients in a single visit. Dr Rawls: One thing that I think is helpful for me is trying to understand where the patients and their families are when they come in. Because some of the patients come in and have no prior inkling that they may have a neurodegenerative illness like Parkinson disease. Some of my patients come in and say, I'm here for a second opinion for Parkinson disease. So, then I have an idea of where we are in regard to potential understanding of how to start the conversation going forward. If it is someone who is coming in and has not heard about Parkinson disease, or their family has not been made aware that that's the one reason why they're coming to see a movement disorder specialist, then I will start at the beginning After we finish our history, do a very thorough physical exam, I will talk about things that I heard in the history and that I see on the physical exam that make me concerned for a disease like Parkinson disease. I make sure to tell them where I'm getting my criteria from and not just start off, I think you have Parkinson, here's your medication. I think that's very jarring when you're talking with patients and their families, particularly if they had no idea that this could be a potential diagnosis on the table. Like I said, I will start off with recounting, this is what I've heard in your history that makes me concerned. This is what I've seen on your physical exam that makes me concerned. And I think you have Parkinson disease and here is why. And I'll tell them about the tenants like we discussed about Parkinson disease, both the motor and nonmotor symptoms that we see. So that's kind of the first part is, I make sure to lay it out and then open the room up for some questions and clarification. The other portion of this is that, when I'm talking about counseling the patient, I say, we do not expect Parkinson disease to decrease your lifespan. However, over time, our persons, because it is a neurodegenerative illnesses will accumulate deficits over time. So, more stiffness, more slowness, more walking problems. They may, if they have tremor, the tremor may become worse. If they don't have tremor, they might develop tremor in the future. If we're talking about the nonmotor symptoms that we talk about, the main ones are going to be issues with urinary problems, issues with bowels, and then the other thing is going to be neuropsychiatric issues like anxiety and depression. And those things become more prominent, usually, the nonmotor symptoms later on in the disease process, and then also cognitive impairment as well. I really want to make sure that they have the information that I'm seeing, and if there's anything that they want to correct on their end, as in they're saying, oh wait, well, actually I noticed something else, then that's usually when that comes out around kind of the wrapping-up portion of the visit. So, I think that's really important to, one, be very clear in what I am seeing and if there's red flags, and then tell them, okay this is not going to shorten your lifespan. However, over time, we do have other issues and problems that will arise and we can support you as best as we can through that. The one thing I also been very open with people about is- because our patients will say, is there anything I can do? What can be done? Is there any medication to slow down or stop things? And I let people know that unfortunately, right now there's not an intervention that slows down, stops, or reverses disease progression, with the exception of exercise. Consistent exercise has been found to help to slow down disease progression, okay? And also, it can help to release the dopamine already being made innately in the brain. And also, it can help with our cardiovascular health in the big thing: being balanced. Core strength, quadricep strength. So that's also something that people can work on that they should. And I let people know that exercise is as important as the medications themselves. Dr Nevel: Absolutely. And it's incredible how much they incorporate exercise into their daily lives and get active, people who weren't active before their diagnosis, and how much that can help. One question that I think patients sometimes ask is, when they understand how carbidopa/levodopa works and what the expectations are for that medication, that it's not a disease-modifying medication, but that it can help with their symptoms. And then they kind of hear, well as time goes on, they need higher doses or, you know, it doesn't control their motor symptoms as well. They'll say, okay well, is it better to wait then? Should I wait to start carbidopa/levodopa? Like in my mind, I'm only maybe going to get X amount of time from carbidopa/levodopa. So, I'd rather wait to start it than start it now. What do you say to them and how do you counsel them through that? Dr Rawls: So that is a common question that I do get with my patients. So, I tell people, I'm here for you. And it really depends on how you feel at this time. Because you have to weigh the risks and benefits of the medication itself. If someone who's very, very mild decides to take the medication, they feel nauseous, they're just going to say, hey, listen, it's not for me right now. I don't feel like I need it, and then stop, which is with definitely within their right. But what I always counsel patients as well is to say, the dopamine-producing neurons in the substantia nigra are starting to die over time. That is why we are getting the signs and symptoms of Parkinson disease. At some point, your brain is not going to produce enough dopamine that is needed for you to move when you want to move and not move when you don't want to move. Okay? Giving you at least the motor symptoms of Parkinson disease. With this, it's not that the medication stops working, it's just that you need more dopamine to help replace the dopamine that's being lost. However, the dopamine that you are taking or levodopa that you're taking orally is not going to be released as consistently as it is in your brain on demand and shut off when you don't need it. Hence the reason we get more motor fluctuations. Also, potential side effects in the medication like orthostatic hypertension, hallucinations, impulse control disorders. Because you're having to take more escalating doses, those side effects can become more prominent and also lead us to have to balance between the side effects and the medication itself. So, it's not that the medication does not work, your body needs more of it. Some people will say, oh, well, I want to wait, and I say, that's completely fine. However, my cutoff is basically saying, if you are finding that you, as the person who's afflicted is not able to get up in the morning like you want to, you're avoiding going to walk your dog or working in your garden, you know, because you feel stiff and feel slow; you're avoiding, you know, going out to the community, having lunch with your friends or your family because you're embarrassed by your tremor; this is something that is keeping you from living your life. And that's the time that we need to strongly consider starting the medications. So, a person afflicted will accumulate deficits. However, it's how much the deficits are going to affect you. So, if it's really affecting your life, we have tools and ways to help mitigate that. Dr Nevel: Yeah, absolutely. Are there any aspects of Parkinson disease management that you feel are maybe underrecognized or perhaps underutilized? In other words, you know, are there things that we the listeners should be maybe more aware of or think about offering or recommending to our patients that you think maybe aren't as much as they could be? Dr Rawls: I will say the nonmotor symptoms---in particular the neuropsychiatric symptoms with the anxiety and depression, usually later on disease process but also can be earlier as well---I think that is going to be something that is recognized but maybe undertreated in a lot of our patient population. I think part of that is also the fluctuations in dopamine that are occurring naturally in the person, but also, our patients, oftentimes with their medication regimen, really have to be on the ball taking the medication. If they're even 15 minutes late, 10 minutes late, 5 minutes late, we're now off, and now we're waiting for it to kick in. And so that can cause a lot of anxiousness even throughout the day. And then knowing that slowly over time that they're going to accumulate these motor and nonmotor deficits can definitely be problematic as well. There is obvious reason for this underlying potential anxiety and depression. And while we do talk about that and bring that up, sometimes patients will say, oh well, I don't think it's a problem right now. I don't have to mess with this. But usually at some point it does become an issue that usually the family members will bring up and saying, hey, you know, my loved one is very anxious. Or I've noticed that they're just really disengaged from what's going on in their lives and they are not talking as much, they're not going out as much. Again, that could be a combination of depression/anxiety, but it also can be a physical- a combination of, I'm not physically able to do these things, or, they're much more difficult for me to initiate doing these activities. I always want to be mindful. If my patients come in and they already have a diagnosis of depression or anxiety and they're already being treated by a mental health counselor, provider, or a psychiatrist, then I will work with providers so that we can try to optimize their medication regimen. The other thing is, well, if this is the first time that they're really being seen by someone and talking about their anxiety and depression, then oftentimes I will have them go back to their primary care and see if maybe an SSRI or SNRI will be helpful to try to help with the neuropsychiatric symptoms they may be experiencing. So that's one big one. Another one that I think that might be a little bit underappreciated is going to be drooling. Sometimes I'll come in and see my patients and notice some drooling that's happening with the mouth being open, not being able to initiate the swallowing reflex consistently throughout the day. Or they may be patting their face a lot with a napkin or a towel and then bringing that up and bringing it to light. Oh yeah. I have a lot of drooling while I'm awake. It's on my shirt. It's embarrassing. I feel like it's a little bit too much for me or my family. We have to put a bib on because I'm just drooling all throughout the day. That can really be uncomfortable and cause skin breakdown. It can also be socially embarrassing. So, there are some tools that I talk to people about with drooling. One thing I start with is going to be using sugar-free gum or candy while the person is awake to help initiate the swallow reflex, and sometimes that's all that's needed. There are other agents that can be used---like glycopyrrolate, sublingual atropine drops, and scopolamine patches---that can help with decreasing saliva production. But there can be side effects of making the entire body feel dry, and then also potential cardiac arrhythmias. If those are not helpful or they're contraindicated with the patient, another thing is going to be botulinum toxin injections. So those can be done on the parotid and salivary glands to decrease the amount of saliva that's being produced. So oftentimes people will come to me, because I'm also a botulinum toxin injector. I've been sent by some of my colleagues to inject our persons that have significant sialorrhea. Dr Nevel: Wonderful. Well, thank you so much for chatting with me today about your article. Again, today I've been interviewing Dr Ashley Rawls about her article on Parkinson disease, which appears in the August 2025 Continuum issue on movement disorders. Be sure to check out Continuum Audio episodes from this and other issues. And thank you to our listeners for joining today. And thank you, Ashley, for sharing all your knowledge with us today. Dr Rawls: Thank you, Kate, I appreciate your time. And have a great day, everyone. Dr Monteith: This is Dr Teshmae Monteith, Associate Editor of Continuum Audio. If you've enjoyed this episode, you'll love the journal, which is full of in-depth and clinically relevant information important for neurology practitioners. Use the link in the episode notes to learn more and subscribe. AAN members, you can get CME for listening to this interview by completing the evaluation at continpub.com/audioCME. Thank you for listening to Continuum Audio.

Join Jay Gunkelman, QEEGD (the man who has analyzed over 500,000 brain scans), and host Pete Jansons for another engaging NeuroNoodle Neurofeedback Podcast episode discussing neuroscience, psychology, mental health, and brain training.✅ Topic 1 Explained: Cold feet during neurofeedback might be linked to sympathetic overarousal or circulation issues—Jay explores temperature training, HRV, and even vascular screenings.✅ Topic 2 Deep Dive: SMR's effect on blood flow and how precise frequency training can improve perfusion, reduce ischemia, and support conditions like migraines and traumatic brain injury.✅ Topic 3 Insights: Restless leg syndrome is examined as a sleep disorder treated with dopamine-based meds and SMR neurofeedback—plus how frontal beta balance prevents underarousal.✅ Additional Topics:

In this episode of ASTCT Talks, Dr. Rahul Banerjee sits down with Dr. Kenneth Lim and Dr. Yi Lin of Mayo Clinic to discuss a critical and emerging topic in CAR T-cell therapy: delayed neurotoxicities following cilta-cel treatment in multiple myeloma. They break down the clinical features of nerve palsies and Parkinsonism-like symptoms, share diagnostic and treatment strategies and explore emerging predictive markers like absolute lymphocyte count. Given that cilta-cel is increasingly being used in second-line myeloma treatment and is even being studied in first-line treatment to replace stem cell transplantation, this conversation is a timely and insightful look at improving patient outcomes in CAR T-cell therapy.

In this exciting interview (watch on YouTube), we sit down with Colonel Philip Blair, MD, (USAF Ret), CEO of Blair Medical Group, to explore the potential of β-caryophyllene (BCP)—a natural, plant-based compound—to support and even transform the treatment of Parkinson's Disease. Dr. Blair brings decades of clinical and military medical experience to the table as he explains how BCP interacts with the endocannabinoid system, reduces inflammation, and may protect neurons—offering real hope for those living with Parkinson's. In this episode, you'll learn: ✅ What is β-caryophyllene (BCP)? ✅ How BCP interacts with CB2 receptors in the brain ✅ The role of inflammation in Parkinson's and how BCP may help ✅ Clinical insights from Dr. Blair's patient experience ✅ Natural healing strategies that go beyond conventional medicine Learn more about Dr. Blair's medical practice and BCP products here (be sure to use promo code PDEDUCATION at checkout for 10% off!): https://www.blairmedicalgroup.shop/?aff=22

Can cannabis really help manage Parkinson's symptoms? In this episode (watch on YouTube), we dive into the science, the possibilities, and the risks. From non-motor symptoms like sleep issues and anxiety to potential interactions with common Parkinson's medications, we break down what CBD and THC might offer. You'll also learn about the many forms of cannabis — including gummies, tinctures, topicals, patches, and more — and which options are most commonly used in Parkinson's care.  We'll also explore important drug interactions with levodopa, dopamine agonists, and antidepressants — plus how to talk to your doctor about trying cannabis safely. Whether you're a person with Parkinson's, a caregiver, or a clinician, this episode offers a balanced, evidence-based look at cannabis as part of a holistic PD care strategy. Access a free printable guide to Cannabis products here: https://pdeducation.thinkific.com/products/digital_downloads/cannabis4pd Help to support this channel and out efforts to educate the world about Parkinson's Disease and get access to personalized content: https://www.youtube.com/channel/UC0g3abv8hkaqZbGD8y1dfYQ/join  https://www.patreon.com/pdeducation  Please be sure to give support to our channel sponsors: Comfort Linen: https://comfortlinen.com/PARKINSONSDISEASEEDUCATION (15% off entire order when applying the code PARKINSONSDISEASEEDUCATION at checkout) Kizik Shoes: https://kizik.sjv.io/pdeducation Cure Hydration: https://lvnta.com/lv_XG06Rho8SSlXEq3qlV If you have products that you would like for me to review on the channel please send them here: Parkinson's Disease Education P.O. Box 1678 Broken Arrow, OK 74013 Medical Disclaimer: All information, content, and material of this video is for informational purposes only and not intended to serve as a substitute for the consultation, diagnosis, and/or medical treatment of a qualified physician or healthcare provider. Affiliate disclaimer: Keep in mind that links used for recommended products may earn me a commission when you make purchases. However, this does not impact what products I recommend. If I recommend a specific product it is because it has been vetted by myself or based on personal use. #parkinson #parkinsonsawareness #parkinsonsdisease #parkinsonsawareness #cannabiseducation #parkinsonssymptoms #movementdisorder #cannabidiol

In this episode, Prof. Tiago Outeiro interviews Prof. William Langston on the intriguing history of drug addicts manifesting parkinsonism in the 1980s, and how MPTP became a tool compound for modeling certain aspects of Parkinson's disease.

Delaying diagnosis of parkinsonism can mean delaying care. In a study recently published in JAMA Neurology, David Vaillancourt, PhD, and colleagues tested the ability of an AI model to differentiate between Parkinson disease and other neurodegenerative disorders when paired with MRI. He joins JAMA and JAMA+ AI Associate Editor Yulin Hswen, ScD, MPH to discuss. Related Content: A Large Proportion of Parkinson Disease Diagnoses Are Wrong—Here's How AI Could Help Automated Imaging Differentiation for Parkinsonism

In this episode (watch on YouTube), we explore the groundbreaking potential of psilocybin—the active ingredient in psychedelic mushrooms—as a promising treatment for Parkinson's disease.

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Welcome to an eye-opening conversation with autophagy practitioner, movement coach, and founder of Genesis Health, Lars Konge, where we dive deep into the science and strategy behind using cellular autophagy to help slow—or even halt—the progression of Parkinson's Disease.

There are so many ways to get involved with Parkinson's disease, from community building to advocacy, research participation to fundraising. Taking that first step toward involvement can be daunting, but many people say it's a critical part of living well with the disease. In this episode of The Michael J. Fox Foundation Parkinson's Podcast, members of the Foundation's Patient Council share stories of their own first steps, explore how engagement has impacted their journeys and offer advice and perspective to others who are looking for ways to make meaningful change. Tune in to hear guest hosts Jimmy Choi, diagnosed with Parkinson's in 2003, and Hadley Ferguson, diagnosed with multiple system atrophy (MSA-P), an atypical Parkinsonism in 2014, reflect on those stories, recorded live in the MJFF offices. Learn more about the many ways to get involved today at michaeljfox.org. Like our podcasts? Please consider leaving a rating or review and sharing the series with your community. https://apple.co/3p02Jw0 The Foundation's landmark study, the Parkinson's Progression Marker's Initiative, also known as PPMI, is recruiting volunteers. Join the study that's changing everything at michaeljfox.org/podcast-ppmi. Mentioned in this episode:The Foundation's landmark research study is exploring the connection between sense of smell and brain disease. People with and without Parkinson's can help by taking a free scratch-and-sniff test. Get yours at mysmelltest.org/request.

Modern medicine has made significant strides in managing chronic diseases, yet many elderly patients with multiple conditions continue to deteriorate under standard care. Conventional therapies often overlook the root causes of chronic degeneration, such as oxidative stress, mitochondrial dysfunction, toxin accumulation, and nutritional deficiencies. IntegrativeOrthomolecular Medicine (IOM) offers a solution-oriented framework that emphasizes restoring biochemical balance through therapeutic nutrition, detoxification, metabolic support, and lifestyle interventions. This case study illustrates the practical application and impressive results of an IOM protocol in an elderly woman with T2DM, CKD with renal insufficiency, Parkinsonism, and recurrent infections.In this episode George discusses the case study of a 94 year old woman who made significant improvements using Orthromolecular nutrition. www.georgebatista.com

Could nicotine—yes, the same compound found in cigarettes—actually help people with Parkinson's Disease?

Can Lion's Mane mushroom help with Parkinson's disease? Research suggests it may support nerve growth, reduce inflammation, and protect dopamine-producing neurons, potentially improving cognitive function and slowing neurodegeneration. Some studies show benefits in Parkinson's models, while human trials highlight its role in memory, focus, and brain health.

Dopamine is essential for movement, mood, and motivation—but did you know that too much dopamine inside of dopamine producing cells can be toxic to those cells? In this episode, we explore dopamine toxicity and its implications for those living with Parkinson's Disease. **The video version contains visuals that could be even more helpful and will enhace your experence of this episode!** We'll cover:

Could a simple drug intended to treat cancer treatment complications be the next big breakthrough in Parkinson's Disease treatment? Dr. Jonathan Sackner-Bernstein, MD, is leading research on tyrosine hydroxylase inhibition as a novel approach to managing Parkinson's symptoms and slowing disease progression. Unlike traditional treatments that focus solely on replacing lost dopamine, a previously FDA approved drug (RB-190) targets tyrosine hydroxylase (TH)—the enzyme responsible for dopamine production—offering a new way to reduce dyskinesias, oxidative stress, and dopamine imbalances in the brain. Watch on YouTube In this episode, we'll break down:  ✅ What tyrosine hydroxylase does and its role in dopamine production ✅ Why too much dopamine in certain brain regions can be problematic ✅ How RB-190 could change the way we treat Parkinson's Disease ✅ The groundbreaking work of Dr. Sackner-Bernstein and what it means for the future If you or a loved one is affected by Parkinson's, this research could be a game-changer! Stay informed about the latest treatments and breakthroughs by liking, subscribing, and turning on notifications. You all will be the FIRST to know when phase IIA of the drug trials start and participants are needed. Follow Dr. Bernstein's blog here: https://www.parkinsonsdisease.blog/

In this exclusive interview, I was honored to sit down with Dr. Jonathan Sackner-Bernstein to discuss his groundbreaking work in the treatment of Parkinson's Disease. (View on YouTube here) As a leading expert and innovator, Dr. Sackner-Bernstein shares insights into the challenges of current therapies, exciting advancements in research, and the potential for transformative treatments that could improve the lives of millions. Do NOT miss this, as he is going to discuss some very exciting news regarding current research for the first time in this interview. Topics covered include: -The limitations of current Parkinson's therapies and the need for innovation. -New approaches being developed to address both motor and non-motor symptoms. -How emerging science is shaping the future of Parkinson's care. This is a must-watch for anyone affected by Parkinson's Disease or interested in the cutting-edge science behind its treatment. Don't forget to like, share, and subscribe for more expert content on Parkinson's Disease and wellness! Follow Dr Bernstein with his blog and sign up for regular updates: https://www.parkinsonsdisease.blog Help to support this channel and out efforts to educate the world about Parkinson's Disease and get access to personalized content: https://www.youtube.com/channel/UC0g3abv8hkaqZbGD8y1dfYQ/join  https://www.patreon.com/pdeducation Please be sure to give support to our channel sponsors: Comfort Linen: https://comfortlinen.com/PARKINSONSDISEASEEDUCATION (15% off entire order when applying the code PARKINSONSDISEASEEDUCATION at checkout) Kizik Shoes: https://kizik.sjv.io/pdeducation Cure Hydration: https://lvnta.com/lv_XG06Rho8SSlXEq3qlV If you have products that you would like for me to review on the channel please send them here: Parkinson's Disease Education P.O. Box 1678 Broken Arrow, OK 74013 Medical Disclaimer All information, content, and material of this video is for informational purposes only and not intended to serve as a substitute for the consultation, diagnosis, and/or medical treatment of a qualified physician or healthcare provider. #parkinson #parkinsonsawareness #parkinsonsdisease #parkinsons #dopamine #medication #research #interview

Could light therapy be a breakthrough for Parkinson's Disease? In this episode (watch on YouTube here), we dive into the science behind Photobiomodulation (PBM) and how it may help manage Parkinson's symptoms. PBM uses red and near-infrared light to stimulate cellular activity, potentially offering benefits such as: ✅ Neuroprotection & Mitochondrial Support – Improves brain cell energy production and reduces oxidative stress.  ✅ Dopamine Preservation – May protect dopamine-producing neurons and slow disease progression.  ✅ Reduced Inflammation – Helps combat neuroinflammation linked to Parkinson's symptoms. ✅ Motor Function Improvement – Could enhance movement, coordination, and balance. ✅ Cognitive & Mood Benefits – May support brain plasticity, mood regulation, and sleep. While early research is promising, more studies are needed to confirm PBM's long-term impact. Could this be the future of Parkinson's treatment? You can find information about LifeWave products here: https://lifewave.com/hylandpt To book a call with me to ask questions or talk about LifeWave use this link: https://calendly.com/pdeducation/lifewave-consultation  Test your knowledge about Parkinson's Disease! Take our free quiz here: https://www.tryinteract.com/share/quiz/66eadc2571c20e90c568e1e1 Help to support this channel and out efforts to educate the world about Parkinson's Disease and get access to personalized content: https://www.youtube.com/channel/UC0g3abv8hkaqZbGD8y1dfYQ/join  https://www.patreon.com/pdeducation  Please be sure to give support to our channel sponsors: Comfort Linen: https://comfortlinen.com/PARKINSONSDISEASEEDUCATION(15% off entire order when applying the code PARKINSONSDISEASEEDUCATION at checkout) Kizik Shoes: https://kizik.sjv.io/pdeducation Cure Hydration: https://lvnta.com/lv_XG06Rho8SSlXEq3qlV If you have products that you would like for me to review on the channel please send them here: Parkinson's Disease Education P.O. Box 1678 Broken Arrow, OK 74013 Medical Disclaimer All information, content, and material of this video is for informational purposes only and not intended to serve as a substitute for the consultation, diagnosis, and/or medical treatment of a qualified physician or healthcare provider. Affiliate disclaimer: Keep in mind that links used for recommended products may earn me a commission when you make purchases. However, this does not impact what products I recommend. If I recommend a specific product it is because it has been vetted by myself or based on personal use #parkinson #parkinsonsawareness #parkinsonsdisease #parkinsons #photobiomodulation #redlighttherapybenefits #mitochondrialhealth #peptides #lifewave

Join us for another Neurofeedback Podcast episode featuring Jay Gunkelman, QEEGD (the man who has read over 500,000 brain scans) and Dr. Mari Swingle (author of i-Minds). Hosted by Pete Jansons, this episode explores operant vs. classical conditioning, the psychology of rewards vs. punishments, and how neurofeedback shapes behavior.

How do doctors diagnose Parkinson's Disease? In this episode (video here), we break down the key tests and evaluations used to identify Parkinson's, including: Clinical Evaluation: A neurologist assesses motor symptoms like tremors, rigidity, and slowness of movement, alongside your medical history. DaTscan: An imaging test that uses a radioactive tracer to visualize dopamine-producing cells in the brain, helping distinguish Parkinson's from other movement disorders. Alpha-Synuclein Tests: Cutting-edge biomarker tests, including spinal fluid analysis and skin biopsies, that detect misfolded alpha-synuclein—a hallmark of Parkinson's. While no single test can confirm Parkinson's, these tools, combined with a doctor's expertise, provide critical insights for diagnosis. Don't forget to like, share, and subscribe for more expert content on Parkinson's Disease research and management! Help to support this channel and out efforts to educate the world about Parkinson's Disease and get access to personalized content: https://www.youtube.com/channel/UC0g3abv8hkaqZbGD8y1dfYQ/join  https://www.patreon.com/pdeducation  Please be sure to give support to our channel sponsors: Comfort Linen: https://comfortlinen.com/PARKINSONSDISEASEEDUCATION (15% off entire order when applying the code PARKINSONSDISEASEEDUCATION at checkout) Kizik Shoes: https://kizik.sjv.io/pdeducation Cure Hydration: https://lvnta.com/lv_XG06Rho8SSlXEq3qlV  If you have products that you would like for me to review on the channel please send them here: Parkinson's Disease Education P.O. Box 1678 Broken Arrow, OK 74013 Medical Disclaimer All information, content, and material of this video is for informational purposes only and not intended to serve as a substitute for the consultation, diagnosis, and/or medical treatment of a qualified physician or healthcare provider. Affiliate disclaimer: Keep in mind that links used for recommended products may earn me a commission when you make purchases. However, this does not impact what products I recommend. If I recommend a specific product it is because it has been vetted by myself or based on personal use

What causes dyskinesia in Parkinson's Disease, and why does it often appear as a side effect of treatment? In this video, we explore the science behind Parkinson's dyskinesia—a condition characterized by involuntary, erratic movements that can significantly impact quality of life. We'll break down: -How long-term use of levodopa (a common Parkinson's medication) can lead to dyskinesia. -The role of dopamine fluctuations and brain receptor changes in causing these movements. -Insights into other contributing factors and strategies for managing dyskinesia effectively. Whether you're living with Parkinson's or supporting someone who is, this video offers a deeper understanding of this challenging symptom and what can be done to address it. Join me in a FREE webinar 5 Top Parkinson's Myths and How to Debunk Them on Jan 8th, Jan 15th, and Jan 17th. Here is the link to register: https://pdeducation.podia.com/webinars Help to support this channel and out efforts to educate the world about Parkinson's Disease and get access to personalized content: https://www.youtube.com/channel/UC0g3abv8hkaqZbGD8y1dfYQ/join  https://www.patreon.com/pdeducation Please be sure to give support to our channel sponsors: Comfort Linen: https://comfortlinen.com/PARKINSONSDISEASEEDUCATION(15% off entire order when applying the code PARKINSONSDISEASEEDUCATION at checkout) Kizik Shoes: https://kizik.sjv.io/pdeducation Cure Hydration: https://lvnta.com/lv_XG06Rho8SSlXEq3qlV If you have products that you would like for me to review on the channel please send them here: Parkinson's Disease Education P.O. Box 1678 Broken Arrow, OK 74013 Medical Disclaimer All information, content, and material of this video is for informational purposes only and not intended to serve as a substitute for the consultation, diagnosis, and/or medical treatment of a qualified physician or healthcare provider. Affiliate disclaimer: Keep in mind that links used for recommended products may earn me a commission when you make purchases. However, this does not impact what products I recommend. If I recommend a specific product it is because it has been vetted by myself or based on personal use #parkinson #parkinsonsawareness #parkinsonsdisease #parkinsons #dyskinesia #dopamine

Did you know that rhinorrhea (runny nose) could be linked to Parkinson's Disease? In this episode (video version here), we uncover the relationship between these seemingly unrelated conditions. Learn why rhinorrhea might occur in Parkinson's patients, how it differs from typical causes like allergies or colds, and what it could reveal about underlying disease mechanisms.  Key topics include:  -What causes rhinorrhea in Parkinson's Disease?  -How autonomic dysfunction and dopamine loss contribute to this symptom.  -Effective strategies for managing rhinorrhea in Parkinson's.  Join us as we explore this unique symptom and its implications for understanding Parkinson's. Don't forget to like, share, and subscribe for more expert insights on Parkinson's Disease and its management.  Test your knowledge about Parkinson's Disease! Take our free quiz here: https://www.tryinteract.com/share/quiz/66eadc2571c20e90c568e1e1 Help to support this channel and out efforts to educate the world about Parkinson's Disease and get access to personalized content: https://www.youtube.com/channel/UC0g3abv8hkaqZbGD8y1dfYQ/join  https://www.patreon.com/pdeducation Please be sure to give support to our channel sponsors:  Comfort Linen: https://comfortlinen.com/PARKINSONSDISEASEEDUCATION (15% off entire order when applying the code PARKINSONSDISEASEEDUCATION at checkout)  Kizik Shoes: https://kizik.sjv.io/pdeducation Cure Hydration: https://lvnta.com/lv_XG06Rho8SSlXEq3qlV If you have products that you would like for me to review on the channel please send them here: Parkinson's Disease Education P.O. Box 1678 Broken Arrow, OK 74013  Medical Disclaimer: All information, content, and material of this video is for informational purposes only and not intended to serve as a substitute for the consultation, diagnosis, and/or medical treatment of a qualified physician or healthcare provider.  Affiliate disclaimer: Keep in mind that links used for recommended products may earn me a commission when you make purchases. However, this does not impact what products I recommend. If I recommend a specific product it is because it has been vetted by myself or based on personal use #parkinson #parkinsonsawareness #parkinsonsdisease #parkinsons #runnynose

In this episode of Discovery Matters we delve into groundbreaking advancements in Parkinson's disease research. Dodi and Conor transport us to the frontier of medical innovation, exploring the latest discoveries and techniques that hold promise for early diagnosis and treatment of Parkinson's disease. Show notes • Decet, Marianna et al. ‘A candidate loss-of-function variant in SGIP1 causes synaptic dysfunction and recessive parkinsonism', Cell Reports Medicine, Volume 5, Issue 10. • Hällqvist, J., Bartl, M., Dakna, M. et al. ‘Plasma proteomics identify biomarkers predicting Parkinson's disease up to 7 years before symptom onset'. Nat Commun 15, 4759 (2024). • Roald Dahl's Marvellous Children's Charity Keywords: non-invasive procedure, early diagnosis, synaptic homeostasis, Parkinsonism, biomarkers, machine learning, REM sleep disorder, inflammatory pathways, dopaminergic cells, predictive diagnostics, early intervention.

Exercise is crucial for managing Parkinson's Disease, but what if you're battling fatigue? In this video, we dive into strategies to stay active without overexerting yourself. Learn how to tailor your exercise routine to improve strength, balance, and mobility while managing your energy effectively. Video version is here. Key topics include: -Why fatigue happens in Parkinson's and how exercise can help. -The best types of low-impact exercises for maintaining energy levels. -Tips for pacing, recovery, and avoiding burnout during workouts. Find out how to build a sustainable fitness plan that works for you and supports your fight against Parkinson's symptoms. Subscribe for more expert advice on living well with Parkinson's Disease.  Help to support this channel and out efforts to educate the world about Parkinson's Disease and get access to personalized content:  https://www.youtube.com/channel/UC0g3abv8hkaqZbGD8y1dfYQ/join https://www.patreon.com/pdeducation Please be sure to give support to our channel sponsors:  Comfort Linen: https://comfortlinen.com/PARKINSONSDISEASEEDUCATION (15% off entire order when applying the code PARKINSONSDISEASEEDUCATION at checkout)  Kizik Shoes: https://kizik.sjv.io/q4y1RL Cure Hydration: https://lvnta.com/lv_XG06Rho8SSlXEq3qlV If you have products that you would like for me to review on the channel please send them here: Parkinson's Disease Education P.O. Box 1678 Broken Arrow, OK 74013  Medical Disclaimer All information, content, and material of this video is for informational purposes only and not intended to serve as a substitute for the consultation, diagnosis, and/or medical treatment of a qualified physician or healthcare provider.  Affiliate disclaimer: Keep in mind that links used for recommended products may earn me a commission when you make purchases. However, this does not impact what products I recommend. If I recommend a specific product it is because it has been vetted by myself or based on personal use #parkinson #parkinsonsawareness #parkinsonsdisease #parkinsons #exercise #fatigue #parkinsonsexercise

Dr. Gordon Smith and Dr. Whitley Aamodt discuss end-of-life care for patients with neurodegenerative diseases, focusing on healthcare utilization, hospice enrollment, and the importance of early conversations about care preferences. Show reference: https://www.neurology.org/doi/10.1212/WNL.0000000000209925    

Dr. Gordon Smith talks with Dr. Whitley Aamodt about the comparison of resource utilization between US Medicare decedents with neurodegenerative diseases and those with cancer. Read the related article in Neurology. Disclosures can be found at Neurology.org.

In the October 2024 replay features four episodes on approaches to clinical diagnosis of parkinsonism. The episode starts off with Dr. Colin Hoy discuss the concept of prodromal Parkinson disease and the ethical considerations surrounding its diagnosis. The episode leads into a conversation with Dr. Chris Gibbons discussing skin biopsies to detect phosphorylated α-synuclein. In the third episode Drs. Michiko K. Bruno and Lawrence Golbe about a practical diagnostic algorithm for atypical parkinsonian disorders Drs. Michiko K. Bruno and Lawrence Golbe discuss a practical diagnostic algorithm for atypical parkinsonian disorders. The episode concludes with Dr. Eduardo De Pablo-Fernández talking about the strengths of DAT imaging in diagnosing patients with Parkinsonian disorders. Previous Podcasts: The Ethical Landscape of Prodromal Parkinson Disease Skin Biopsy Detection of Phosphorylated α-Synuclein General Neurologist's Practical Diagnostic Algorithm for Atypical Parkinsonian Disorders Interpreting DAT Imaging Results in the Clinical Context Article Links: The Ethical Landscape of Prodromal Parkinson Disease  Skin Biopsy Detection of Phosphorylated α-Synuclein in Patients With Synucleinopathies A General Neurologist's Practical Diagnostic Algorithm for Atypical Parkinsonian Disorders  Neuropathologic Validation and Diagnostic Accuracy of Presynaptic Dopaminergic Imaging in the Diagnosis of Parkinsonism Disclosures can be found at Neurology.org.

Megyn Kelly is joined by Batya Ungar-Sargon, author of "Second Class," to discuss where President Joe Biden has been since he's been disappeared by his party, how VP Kamala Harris has essentially replaced him as president, the "ritual humiliation" of Biden by his former friends and colleagues, why elites on the left hate JD Vance, the attempt to reframe the narrative around Harris, how the media is pushing Harris' “vibe” over actual policies, the full context about JD Vance's comments on having kids, the clickbait the left is portraying and the misleading quotes they are pulling, the reality it was a response to the cultural points about the benefits of not having kids, his own powerful family story, Megan Thee Stallion's performance at Kamala Harris' rally in Atlanta, Kid Rock's performance of a pretty raunchy song at the RNC, Megyn reading lyrics of each artist, and more. Then Dr. Drew, host of "Ask Dr. Drew," joins to discuss the ridiculous Pro-Kamala Harris Zoom calls segregated by race, the passive aggressive preachiness on display from the 'white women" call, the disgust that comes from it by the average person, Biden's symptoms and cognitive and physical health issues, how it's obvious he has Parkinsonism, what's going on with Harris' weird word salad answers, the tech censorship of Trump's assassination attempt, and more.Ungar-Sargon- https://www.amazon.com/Second-Class-Betrayed-Americas-Working/dp/1641773618Dr. Drew- https://drdrew.com/Tax Network USA: https://TNUSA.com/MEGYN or call 1-800-245-6000Done with Debt: https://www.donewithdebt.com/Follow The Megyn Kelly Show on all social platforms:YouTube: https://www.youtube.com/MegynKellyTwitter: http://Twitter.com/MegynKellyShowInstagram: http://Instagram.com/MegynKellyShowFacebook: http://Facebook.com/MegynKellyShow Find out more information at: https://www.devilmaycaremedia.com/megynkellyshow

Unleashed: The Political News Hour with Ted Noel MD – Joe Biden's public performances raise concerns about his health, specifically Parkinsonism. Observations of his stiffness, slow gait, and cognitive disturbances suggest severe neurological issues. An anonymous neurologist confirms these signs align with Parkinson's disease. The urgency for diagnosis and treatment is critical, impacting Biden's ability to fulfill presidential duties effectively.